title: A two-step toward personalized therapies for prostate cancer.
abstract: Identifying the dominant genetic alterations that drive tumorigenesis is essential for developing targeted cancer therapies. Recent work has demonstrated that prostate tumors can be stratified by dominant genetic alterations, such as chromosomal rearrangements involving ETS (Erythroblastosis virus E26 transformation-specific) family transcription factors or overexpression of SPINK1, a gene that encodes a secreted serine protease inhibitor. In this issue of Science Translational Medicine, Ateeq et al. provide evidence to support a rationale for targeting the SPINK1 protein in the SPINK1+/ETS⁻ subset of prostate tumors and also describe a potential interaction of SPINK1 with epidermal growth factor receptor that could be an additional target for therapeutic intervention.
authors.affiliation: Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA.
authors.forename: Andrew S
authors.initials: AS
authors.lastname: Goldstein
authors.forename: Yang
authors.initials: Y
authors.lastname: Zong
authors.forename: Owen N
authors.initials: ON
authors.lastname: Witte
mesh_terms: D000818:Animals; D014408:Biomarkers, Tumor / Q000235:genetics / Q000378:metabolism; D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism; D066246:ErbB Receptors / Q000378:metabolism; D018390:Gene Targeting; D006801:Humans; D008297:Male; D057285:Precision Medicine; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000628:therapy*; D015398:Signal Transduction; D014359:Trypsin Inhibitor, Kazal Pancreatic
chemical_list: D014408:Biomarkers, Tumor; D002352:Carrier Proteins; C486642:SPINK1 protein, human; D014359:Trypsin Inhibitor, Kazal Pancreatic; D066246:ErbB Receptors